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Effect of Co‐culture with Pulmonary Arterial Endothelial Cells on Phenotype of Pulmonary Arterial Smooth Muscle Cells
Author(s) -
Gairhe Salina,
Bauer Natalie,
Grethoffer William,
McMurtry Ivan Fredrick
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.769.3
Subject(s) - phenotype , paracrine signalling , vascular smooth muscle , microbiology and biotechnology , endothelium , biology , cancer research , pathology , chemistry , medicine , smooth muscle , endocrinology , receptor , gene , biochemistry
Pulmonary arterial smooth muscle cells (PASMCs) work in concert with pulmonary arterial endothelial cells (PAECs) to maintain the homeostasis of pulmonary arteries. Injury and pathological conditions alter PASMCs to a de‐differentiated/synthetic phenotype, most likely dependent on the endothelium. The interactions between PAECs and PASMCs and the role of these interactions in modulating PASMC phenotype are not yet understood. To this end, we co‐cultured PASMCs with either PAECs or PASMCs, as a control, on a transwell insert such that the cells can make direct contact with each other through 0.4µm pores in the membrane of the insert. After 48 hrs of co‐culture, PAECs and PASMCs were processed for confocal imaging or collected for western analysis. Morphologically, PASMCs co‐cultured with PAECs were more elongated and spindle shaped than control. Also, in co‐culture with PAECs, PASMCs showed higher expression of the contractile smooth muscle cell (SMC) markers than did control. PASMCs co‐cultured with PAEC developed a more contractile‐like phenotype and resembled the characteristics of SMCs in normal pulmonary arteries. Collectively, these results suggest that coordinated interaction between PASMCs and PAECs is important in maintaining a contractile PASMC phenotype, and future experiments will investigate the roles of paracrine factors and direct myoendothelial contact. Supported by NIH P01 HL014985.